Chronic Kidney Disease and Disproportionally Increased Cardiovascular Damage: Does Oxidative Stress Explain the Burden?

Figure 1

Pathways of amplified oxidative stress in CKD and byproducts leading to accelerated atherosclerosis. AT: angiotensin; DM: diabetes mellitus; eNOS: endothelial nitric oxide synthase; FAPPs: fatty acid peroxidation products; GSH: glutathione; HT: hypertension; MDA: malondialdehyde; Mito: mitochondria; MPO: myeloperoxidase; NF-κB: nuclear factor kappa-light-chain-enhancer of activated B cells; NOX: NADPH oxidase; NRF2: nuclear factor E2-related factor 2; OxPLs: oxidized phospholipids; PON: paraoxonase; SOD: superoxide dismutase; WBC: white blood cells; XO: xanthine oxidase.